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Isolation and characterization of HTLV-I from symptomatic family members with tropical spastic paraparesis (HTLV-I
G McKhann1, C J Gibbs, C A Mora
1Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland.
Abstract:
Human T lymphotropic virus type I (HTLV-I) was isolated from peripheral blood- and cerebrospinal fluid-derived mononuclear cells of a 13-y-old boy and from the peripheral blood lymphocytes of both his parents. All three had IgG antibodies to HTLV-I and varying degrees of the clinical features of tropical spastic paraparesis (TSP). The son also had IgM antibodies specific for HTLV-I in his serum. Isolations were successfully made from peripheral blood lymphocytes and cerebrospinal fluid lymphocytes stimulated with interleukin-2 or cocultivated with umbilical cord blood mononuclear cells. Established cell lines contained HTLV-I antigen by immunfluorescence and cell-associated virus by electron microscopy; cells became transformed in vitro as determined by their continuous growth in the absence of exogenous interleukin-2. This boy is the youngest TSP patient known to be reported, and the isolation of HTLV-I from all three family members suggests the causative role of this virus in TSP.
Insights
Human T lymphotropic virus type I (HTLV-I) was isolated from a young boy and his parents, all exhibiting symptoms of tropical spastic paraparesis (TSP). This family-wide HTLV-I infection strongly suggests the virus causes TSP.
Area of Science:
- Virology
- Neurology
- Immunology
Background:
- Human T lymphotropic virus type I (HTLV-I) is a retrovirus known to cause neurological diseases.
- Tropical spastic paraparesis (TSP) is a debilitating neurological disorder linked to HTLV-I infection.
Observation:
- HTLV-I was isolated from a 13-year-old boy and his parents, all presenting with clinical features of TSP.
- The boy, the youngest reported TSP patient, showed both IgG and IgM antibodies to HTLV-I.
- Virus isolation was successful from peripheral blood and cerebrospinal fluid lymphocytes.
Findings:
- Established cell lines from the patients showed HTLV-I antigen and virus particles.
- Cells demonstrated in vitro transformation, indicating viral oncogenesis.
- The presence of HTLV-I in all three affected family members supports its etiological role in TSP.
Implications:
- This study provides strong evidence for HTLV-I as the causative agent of TSP.
- Identifying HTLV-I in such a young patient highlights the potential for early-onset neurological disease.
- The findings underscore the importance of diagnosing HTLV-I in individuals with TSP and their families.